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Regular Finnish sauna use is associated with a reduced risk of cardiovascular mortality. However, physiological mechanisms underlying this association remain unknown. This study determined if an 8-wk Finnish sauna intervention improves peripheral endothelial function, microvascular function, central arterial stiffness, and blood pressure in adults with coronary artery disease (CAD). Forty-one adults (62 ± 6 yr, 33 men/8 women) with stable CAD were randomized to 8 wk of Finnish sauna use ( n = 21, 4 sessions/wk, 20-30 min/session, 79°C, 13% relative humidity) or a control intervention ( n = 20, lifestyle maintenance). Brachial artery flow-mediated dilation (FMD), carotid-femoral pulse wave velocity (cf-PWV), total (area under the curve) and peak postocclusion forearm reactive hyperemia, and blood pressure (automated auscultation) were measured before and after the intervention. After the sauna intervention, resting core temperature was lower (-0.27°C [-0.54, -0.01], P = 0.046) and sweat rate during sauna exposure was greater (0.3 L/h [0.1, 0.5], P = 0.003). The change in brachial artery FMD did not differ between interventions (control: 0.07% [-0.99, +1.14] vs. sauna: 0.15% [-0.89, +1.19], interaction P = 0.909). The change in total ( P = 0.031) and peak ( P = 0.024) reactive hyperemia differed between interventions due to a nonsignificant decrease in response to the sauna intervention and an increase in response to control. The change in cf-PWV ( P = 0.816), systolic ( P = 0.951), and diastolic ( P = 0.292) blood pressure did not differ between interventions. These results demonstrate that four sessions of Finnish sauna bathing per week for 8 wk does not improve markers of vascular health in adults with stable CAD. NEW & NOTEWORTHY This study determined if unsupervised Finnish sauna bathing for 8 wk improves markers of vascular health in adults with coronary artery disease. Finnish sauna bathing reduced resting core temperature and improved sweating capacity, indicative of heat acclimation. Despite evidence of heat acclimation, Finnish sauna bathing did not improve markers of endothelial function, microvascular function, arterial stiffness, or blood pressure.

Heat therapy is a promising strategy to improve cardiometabolic health. This study evaluated the acute physiological responses to hot water immersion in adults with type 2 diabetes mellitus (T2DM). On separate days in randomized order, 13 adults with T2DM [8 males/5 females, 62 ± 12 yr, body mass index (BMI): 30.1 ± 4.6 kg/m 2 ] were immersed in thermoneutral (34°C, 90 min) or hot (41°C, core temperature ≥38.5°C for 60 min) water. Insulin sensitivity was quantified via the minimal oral model during an oral glucose tolerance test (OGTT) performed 60 min after immersion. Brachial artery flow-mediated dilation (FMD) and reactive hyperemia were evaluated before and 40 min after immersion. Blood samples were drawn to quantify protein concentrations and mRNA levels of HSP70 and HSP90, and circulating concentrations of cytokines. Relative to thermoneutral water immersion, hot water immersion increased core temperature (+1.66°C [+1.47, +1.87], P < 0.01), heart rate (+34 beats/min [+24, +44], P < 0.01), antegrade shear rate (+96 s -1 [+57, +134], P < 0.01), and IL-6 (+1.38 pg/mL [+0.31, +2.45], P = 0.01). Hot water immersion did not exert an acute change in insulin sensitivity (-0.3 dL/kg/min/μU/mL [-0.9, +0.2], P = 0.18), FMD (-1.0% [-3.6, +1.6], P = 0.56), peak (+0.36 mL/min/mmHg [-0.71, +1.43], P = 0.64), and total (+0.11 mL/min/mmHg × min [-0.46, +0.68], P = 0.87) reactive hyperemia. There was also no change in eHSP70 ( P = 0.64), iHSP70 ( P = 0.06), eHSP90 ( P = 0.80), iHSP90 ( P = 0.51), IL1-RA ( P = 0.11), GLP-1 ( P = 0.59), and NF-κB ( P = 0.56) after hot water immersion. The physiological responses elicited by hot water immersion do not acutely improve markers of cardiometabolic function in adults with T2DM. NEW & NOTEWORTHY Heat therapy has been shown to improve markers of cardiometabolic health in preclinical and clinical studies. However, the effects of heat therapy in individuals with type 2 diabetes mellitus (T2DM) remain understudied. We examined the acute effect of hot water immersion on glucose tolerance, flow-mediated dilation, reactive hyperemia, inflammatory markers, and heat shock proteins in adults with T2DM. Hot water immersion did not acutely improve the markers studied.

Human thermoregulatory control is often evaluated through the relationship between thermoeffector output and core or mean body temperature. In addition to providing a general indication of whether a variable of interest alters thermoregulatory control, this relationship is often used to determine how this alteration may occur. This latter interpretation relies upon two parameters of the thermoeffector output-body temperature relationship: the onset threshold and thermosensitivity. Traditionally, changes in the onset threshold and thermosensitivity are interpreted as "central" or "peripheral" modulation of thermoregulatory control, respectively. This mini-review revisits the origins of the thermoeffector output-body temperature relationship and its use to interpret "central" or "peripheral" modulation of thermoregulatory control. Against this background, we discuss the strengths and weaknesses of this approach and highlight that "central" thermoregulatory control reflects the neural control of body temperature whereas "peripheral" thermoregulatory control reflects properties specific to the thermoeffector organs. We highlight studies that employed more direct approaches to investigate the neural control of body temperature and peripheral properties of thermoeffector organs. We conclude by encouraging future investigations interested in studying thermoregulatory control to more directly investigate the component of the thermoeffector loop under investigation.heat; human; skin blood flow; sweat; thermoregulatory.

This study assessed whether, notwithstanding lower resting absolute core temperatures, alterations in time-dependent changes in thermoregulatory responses following partial and complete heat acclimation (HA) are only evident during uncompensable heat stress. Eight untrained individuals underwent 8 wk of aerobic training (i.e., partial HA) followed by 6 days of HA in 38°C/65% relative humidity (RH) (i.e., complete HA). On separate days, esophageal temperature (T es ), arm (LSR arm ), and back (LSR back ) sweat rate, and whole body sweat rate (WBSR) were measured during a 45-min compensable (37°C/30% RH) and 60-min uncompensable (37°C/60% RH) heat stress trial pre-training (PRE-TRN), post-training (POST-TRN), and post-heat acclimation (POST-HA). For compensable heat stress trials, resting T es was lower POST-TRN (36.74 ± 0.27°C, P = 0.05) and POST-HA (36.60 ± 0.27°C, P = 0.001) compared with PRE-TRN (36.99 ± 0.19°C); however, ΔT es was similar in all trials (PRE-TRN:0.40 ± 0.23°C; POST-TRN:0.42 ± 0.20°C; POST-HA:0.43 ± 0.12°C, P = 0.97). While LSR back was unaltered by HA ( P = 0.94), end-exercise LSR arm was higher POST-TRN (0.70 ± 0.14 mg·cm -2 ·min -1 , P < 0.001) and POST-HA (0.75 ± 0.16 mg·cm -2 ·min -1 , P < 0.001) compared with PRE-TRN (0.61 ± 0.15 mg·cm -2 ·min -1 ). Despite matched evaporative heat balance requirements, steady-state WBSR (31st-45th min) was greater POST-TRN (12.7 ± 1.0 g/min, P = 0.02) and POST-HA (12.9 ± 0.8 g/min, P = 0.004), compared with PRE-TRN (11.7 ± 0.9 g/min). For uncompensable heat stress trials, resting T es was lower POST-TRN (36.77 ± 0.22°C, P = 0.05) and POST-HA (36.62 ± 0.15°C, P = 0.03) compared with PRE-TRN (36.86 ± 0.24°C). But ΔT es was smaller POST-TRN (0.77 ± 0.19°C, P = 0.05) and POST-HA (0.75 ± 0.15°C, P = 0.04) compared with PRE-TRN (1.10 ± 0.32°C). LSR back and LSR arm increased with HA ( P < 0.007), supporting the greater WBSR with HA (POST-TRN:14.4 ± 2.4 g/min, P < 0.001; POST-HA:16.8 ± 2.8 g/min, P < 0.001) compared with PRE-TRN (12.7 ± 3.2 g/min). In conclusion, the thermal benefits of HA are primarily evident when conditions challenge the physiological capacity to dissipate heat. NEW & NOTEWORTHY We demonstrate that neither partial nor complete heat acclimation alters the change in core temperature during compensable heat stress compared with an unacclimated state, despite a marginally greater whole body sweat rate. However, the greater local and whole body sweat rate with partial and complete heat acclimation reduced the rise in core temperature during 60 min of uncompensable heat stress compared with an unacclimated state, suggesting the improvements in heat dissipation associated with heat acclimation are best observed when the upper physiological limits for evaporative heat loss are challenged.

Some studies have observed a functional relationship between sweating and skin blood flow. However, the implications of this relationship during physiologically relevant conditions remain unclear. We manipulated sudomotor activity through changes in sweating efficiency to determine if parallel changes in vasomotor activity are observed. Eight young men completed two trials at 36°C and two trials at 42°C. During these trials, air temperature remained constant while ambient vapor pressure increased from 1.6 to 5.6 kPa over 2 h. Forced airflow across the skin was used to create conditions of high (HiS eff ) or low (LoS eff ) sweating efficiency. Local sweat rate (LSR), local skin blood flow (SkBF), as well as mean skin and esophageal temperatures were measured continuously. It took longer for LSR to increase during HiS eff at 36°C (HiS eff : 99 ± 11 vs. LoS eff : 77 ± 11 min, P < 0.01) and 42°C (HiS eff : 72 ± 16 vs. LoS eff : 51 ± 15 min, P < 0.01). In general, an increase in LSR preceded the increase in SkBF when expressed as ambient vapor pressure and time for all conditions ( P < 0.05). However, both responses were activated at a similar change in mean body temperature (average across all trials, LSR: 0.26 ± 0.15 vs. SkBF: 0.30 ± 0.18°C, P = 0.26). These results demonstrate that altering the point at which LSR is initiated during heat exposure is paralleled by similar shifts for the increase in SkBF. However, local sweat production occurs before an increase in SkBF, suggesting that SkBF is not necessarily a prerequisite for sweating., (Copyright © 2017 the American Physiological Society.)

This study sought to assess the within-subject influence of acute hypoxia on exercise-induced changes in core temperature and sweating. Eight participants [1.75 (0.06) m, 70.2 (6.8) kg, 25 (4) yr, 54 (8) ml·kg -1 ·min -1 ] completed 45 min of cycling, once in normoxia (NORM; [Formula: see text] = 0.21) and twice in hypoxia (HYP1/HYP2; [Formula: see text]= 0.13) at 34.4(0.2)°C, 46(3)% RH. These trials were designed to elicit 1 ) two distinctly different %V̇o 2peak [NORM: 45 (8)% and HYP1: 62 (7)%] at the same heat production (H prod ) [NORM: 6.7 (0.6) W/kg and HYP1: 7.0 (0.5) W/kg]; and 2 ) the same %V̇o 2peak [NORM: 45 (8)% and HYP2: 48 (5)%] with different H prod [NORM: 6.7 (0.6) W/kg and HYP2: 5.5 (0.6) W/kg]. At a fixed %V̇o 2peak , changes in rectal temperature (ΔT re ) and changes in esophageal temperature (ΔT es ) were greater at end-exercise in NORM [ΔT re : 0.76 (0.19)°C; ΔT es : 0.64 (0.22)°C] compared with HYP2 [ΔT re : 0.56 (0.22)°C, P < 0.01; ΔT es : 0.42 (0.21)°C, P < 0.01]. As a result of a greater H prod ( P < 0.01) in normoxia, and therefore evaporative heat balance requirements, to maintain a similar %V̇o 2peak compared with hypoxia, mean local sweat rates (LSR) from the forearm, upper back, and forehead were greater (all P < 0.01) in NORM [1.10 (0.20) mg·cm -2 ·min -1 ] compared with HYP2 [0.71 (0.19) mg·cm -2 ·min -1 ]. However, at a fixed H prod , ΔT re [0.75 (0.24)°C; P = 0.77] and ΔT es [0.63 (0.29)°C; P = 0.69] were not different in HYP1, compared with NORM. Likewise, mean LSR [1.11 (0.20) mg·cm -2 ·min -1 ] was not different ( P = 0.84) in HYP1 compared with NORM. These data demonstrate, using a within-subjects design, that hypoxia does not independently influence thermoregulatory responses. Additionally, further evidence is provided to support that metabolic heat production, irrespective of %V̇o 2peak , determines changes in core temperature and sweating during exercise. NEW & NOTEWORTHY Using a within-subject design, hypoxia does not independently alter core temperature and sweating during exercise at a fixed rate of heat production. These findings also further contribute to the development of a methodological framework for assessing differences in thermoregulatory responses to exercise between various populations and individuals. Using the combined environmental stressors of heat and hypoxia we conclusively demonstrate that exercise intensity relative to aerobic capacity (i.e., %V̇o 2max ) does not influence changes in thermoregulatory responses., (Copyright © 2017 the American Physiological Society.)